Elevated tumor expression of B7-H1 (also known as PD-L1) is predictive of an aggressive disease course, including increased risk of progression and cancer-related death (Thompson et al., Cancer Res 66:3381-3385, 2006; and Zang and Allison, Clin Cancer Res 13:5271-5279, 2007). Retrospective studies suggested that tumors exploit B7-H1 expression to inhibit host T cell function, thereby fostering malignant progression. The concept of tumor B7-H1-mediated immune evasion was an impetus for implementing B7-H1 blockade as a tumor immunotherapy (Zang and Allison, supra; Zou and Chen, Nat Rev Immunol 8:467-477, 2008, Dong and Chen, J Mol Med 81:281-287, 2003; Li et al., Clin Cancer Res 15:1623-1634, 2009; and Webster et al., J Immunol 179:2860-2869, 2007). B7-H1 blockade can dramatically improve tumor immunotherapy by increasing the function of effector CD8 T cells (Strome et al., Cancer Res 63:6501-6505, 2003; Hirano et al., Cancer Res 65:1089-1096, 2005; Blank et al., Int J Cancer 119:317-327, 2006; and Iwai et al., Proc Natl Acad Sci USA 99:12293-12297, 2002). Preclinical studies also provided evidence that B7-H1 blockade may be useful as a treatment for advanced human solid cancers (Dong and Chen, supra; Brahmer et al., New Engl J Med 366:2455-2465, 2012; and Dong and Chen, Cell Mol Immunol 3:179-187, 2006). In these studies, however, only a small portion of treated patients exhibited lasting objective responses (Brahmer et al., supra).